Monday, February 23, 2015

Interpret the ECG shown in Figure 1 — obtained from a middle-aged adult.

Are there DeWinter T waves in the chest leads of Figure-1? Is this patient about to occlude his proximal LAD (Left Anterior Descending) coronary artery?

OR — Does this patient have hyperkalemia?

HINT: What is missing (that should never be missing)?

Figure 1: ECG obtained from a middle-aged adult. Are these DeWinter T waves? Does the patient have hyperkalemia?NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.

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Systematic Interpretation of Figure 1:There is some baseline movement with slight artifact. The overall rhythm is regular — with upright P waves in lead II, so that the rhythm is SinusTachycardia. The rate is ~160/minute (the R-R interval is just under 2 large boxes in duration).

The PR interval is normal — and the QRS complex is narrow. The QT interval is probably normal given the exceedingly rapid heart rate.

The axis is indeterminate (QRS complexes are nearly isoelectric in virtually all limb leads).

There is no chamber enlargement.

Regarding Q-R-S-T Changes:

There appears to be a Q wave in lead aVL.

Transition is slightly delayed to between V4-to-V5 (as the point where the R wave becomes taller than the S wave is deep).

The most remarkable finding on this tracing are the rather tall and peakedT waves, especially in leads V2-thru-V4. In a patient with chest pain — this appearance resembles that of the DeWinter T waves that herald proximal LAD occlusion. There is even suggestion of some J-point ST depression in leads V3,V4 and V5 prior to the steep rise in T wave ascent. In a patient predisposed to hyperkalemia — the T wave peaking seen here should also prompt consideration of this electrolyte disorder.

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QUESTION:What is missing from this presentation?

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ANSWER:No history was given ...

It turns out that this 12-lead ECG was recorded as part of an exercise stress test on an otherwise healthy and asymptomatic middle-aged man. The purpose of this test was to assess exercise capacity. There was no chest pain — and no history of renal disease or other medical problems.

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The LESSON to Be Learned:ECGs cannot be intelligently interpreted in a vacuum. If told that this patient was having new-onset worrisome chest pain — We would wonder why he is so tachycardic, and we would clearly be concerned that the prominent T wave peaking might be ischemic or a DeWinter T wave equivalent. We would check serum K+ values as part of our evaluation, especially if the patient had any factors potentially predisposing to hyperkalemia.

T wave peaking as seen here commonly occurs in healthy adults during exercise. This T wave change is transient — and resolves after termination of exercise.

Rapid-upsloping ST segment depression as seen here in several chest leads is a normal response to exercise.

This patient had excellent exercise capacity for his age. His exercise test was entirely normal — and he was cleared to perform vigorous aerobic activity. No laboratory testing was done (as none was necessary).

My goal in this 58-minute video series is to review the approach to diagnosing the AV Blocks. This starts with recognizing what AV Block is (and is not) — what conditions may mimic AV Block (ie, blocked PACs) — and how to distinguish Complete AV Block from AV Dissociation. Focus is on the 3 types of 2nd-Degree AV Block (Mobitz I; Mobitz II; 2-to-1 AV Block) — and on how to make a definitive diagnosis of Complete AV Block.

Below in Figure 1 — a sample of some issues discussed. I believe this video brings the topic to life!

Figure-1:Slide reviewing the causes of AV Dissociation. The tracing illustrates Sinus Bradycardia with resultant AV Dissociation by "default" (ie, due to slowing of the sinus rate).NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.

Thursday, January 22, 2015

As a source of tracings for practice and/or teaching — I have decided to LINK all ECGs I have commented on as ContributingExpert for ECG Guru (www.ecgguru.com). This may take me several weeks to complete ... I will post the relevant tracing and case on my ECG Blog according to subject— with direct link to My Comment on the ECG Guru.

NOTE: The ECG Guru is dedicated to providing free resources for ECG Teachers and their Students. Search the ECG Guru site if you ever are in need of cases on a particular subject.

Sunday, January 18, 2015

As a source of tracings for practice and/or teaching — I have decided to LINK all ECGs I have commented on as ContributingExpert for ECG Guru (www.ecgguru.com). This may take me several weeks to complete ... I will post the relevant tracing and case on my ECG Blog according to subject— with direct link to My Comment on the ECG Guru.

NOTE: The ECG Guru is dedicated to providing free resources for ECG Teachers and their Students. Search the ECG Guru site if you ever are in need of cases on a particular subject.

Tuesday, December 23, 2014

BE AWARE: This is a highly advanced ECG post that supplements my ECG Video-7. The
essential concepts to master were presented in the Video. But for those of you
who want more — this post hopefully takes assessment of this fascinating case
to a new level! Your feedback and comments are welcome!

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In ECG Blog #101
( = ECG Video-7) — We presented the
case of a 70-year old woman with new-onset
chest pain and the WCT (Wide-Complex Tachycardia) seen in the ECG shown in Figure-1. We posed the following
questions:

What is the rhythm in the long lead II
shown in Figure-1?

Is this VT? If you think it is — How certain are you of your diagnosis?

Our animated Answer to these
questions was covered in detail in our ECG Video-7.

Our purpose in this follow-upECG Blog #102 — is to address the point
highlighted by one of our followers (Алексей Рукин) — regarding the value of meticulous
comparison of the WCT tracing in Figure-1
with the post-conversion ECG.

Figure-1:Initial 12-lead ECG and long lead II rhythm strip obtained from a 70-year old woman with chest pain. Is this VT? How certain are you of your rhythm diagnosis? (Figure reproduced from ECG Video-7). NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.

Discussion of Figure 1:Summary of ECG Video-7

Although the
70-year old woman in this case was hemodynamically stable at the time the
tracing in Figure-1 was obtained — she was having chest pain. Therefore — a quick decision needed to be made as to
whether immediate cardioversion was
indicated.

Definitive
rhythm diagnosis need not be made
initially. Instead — the emergency providers in this case rapidly recognized
from the long lead II rhythm strip that the predominant rhythm was a regularWCTwithout normal sinus P waves. Statisticalodds that this rhythm was VT (Ventricular
Tachycardia) — were at
least 90%. In a 70-year old woman with new chest pain — the appropriate
decision was immediate cardioversion.
This resulted in conversion to sinus rhythm (as we will see momentarily in the post-conversion tracing inFigure-3).

PEARL: Total time to arrive at the decision
to immediately cardiovert this
patient given the above history and the ECG shown in Figure-1 should be no more than seconds …

One of the major
points emphasized in ECG Video-7 — was the presence of a number of additionalclues in Figure-1 that
increase the likelihood that the rhythm is VT to virtually 100%.

Feel free to
take one more look at Figure-1 to see how many of these clues you can identify. Our answers follow below —
which we illustrate in our labeled Figure-2.

Figure-2We have labeled Figure-1 to illustrate additional clues that make diagnosis of VT a virtual certainty.

Discussion of Figure 2:Proof that the Rhythm is indeed VT

As emphasized in
ECG Video-7 — atrial activity is present (at least some of the time) in the long lead II rhythm strip. REDarrows highlight sinusP waves that we see. While the rapid
rate, QRS widening and ST-T wave abnormalities prevent us from marching out P
waves throughout this entire long lead II rhythm strip — regularity of the P
waves we do see (red arrows) —
suggests that there is an underlyingsinus rhythm at a rate of ~130/minute.

Among the most
helpful clues for confirming that a wide tachycardia is VT — is the presence of
one or more of 3 related ECG signs. These are: i) AV dissociation; ii)Capture beats; andiii)Fusion
beats. All 3 of these ECG signs are present in Figure-2 — which proves this rhythm is VT.

AV Dissociation
is present in Figure-2 — because there is an underlying sinus rhythm (suggested
by the red arrows) that is unrelated
to the wide tachycardia (ie, the P waves
= [red arrows] that precede beat #3
and follow beats #7,8,15 are not being conducted).

The QRS complex
is narrow for beats #2, 10, 19 and 23. Each of these beats is preceded by a
sinus P wave. Therefore — beats #2,10,19,23 are all CaptureBeats (in which a sinus P wave occurs at just the right point in the cycle to
get through the AV Node and “capture” the ventricles).

Beat #11 is a FusionBeat. We recognize this because both QRS and T wave morphology of beat
#11 is intermediate between sinus-conducted beats (like beat #10) andventricular beats (like beat #12). That beat #11 is a fusion beat is perhaps best seen within the BLUE rectangle in lead
aVF. (IF beat #10 and beat #12 “had children”
— the offspring might be expected to look
like beat #11, which represents “fusion”
between the morphology of beats #10 and #12).

KEY POINT: — Assessment of QRS Morphology and determination of Axisduringtachycardia are 2 additional features that confirm (with virtual certainty) that the rhythm is VT. To facilitate assessment
of QRS morphology in each of the 12-leads on this tracing — We have placed a “V”
above those beats that are ventricular in each lead.

Note how simultaneousrecording of a long lead II rhythm stripbelow the 12-lead ECG
facilitates determination of which beats are sinus conducted (ie, capture
beats) — and which beats are ventricular ( = the several short runs of NSVT = NonSustainedVT).

The presence of extremeAxis Deviation (ie, the finding of an
allnegative QRS in either lead I or lead aVF) is rare with supraventricular
rhythms. Thus, the all negative QRS complex within
the GREEN rectangle in lead I of Figure-2 by itself virtually proves the
rhythm is VT.

RegardingQRS Morphology: The 3 KEY
leads for assessing the presence and type of BBB (Bundle Branch Block) are leads I, V1 and V6.
Aberrancy almost always manifests QRS morphology consistent with some form of conduction defect (ie, RBBB with or without a hemiblock; or LBBB).
Therefore — the presence of QRS morphology that is inconsistent with some type
of conduction defect makes aberrant conduction or preexisting BBB less
likely (although it does not completely
rule it out).

In Figure-2 — the wide terminal S wave in lead V6 is
consistent with RBBB. However, the amorphous and widened R wave in lead V1 that
ends with an S wave rather than an R’ is not at all suggestive of RBBB — and,
the all negative QRS in lead I is unlike any form of BBB. Thus, QRS morphology
strongly suggests the rhythm is VT.

A
Reason
for VT? A final clue that this rhythm is VT is
contained within the RED rectangles
shown in leads II and III of Figure-2. Note the subtle-but-real small q waves and suggestion of hyperacute ST elevation (especially in lead II) in this 70-year
old woman who presented with new-onset
chest pain.

As was later confirmed on cardiac catheterization — this patient
had acute occlusion of a dominant LCx (left
circumflex) artery — so, her acute inferior
STEMI (STElevation Myocardial
Infarction) clearly provides a “reason” for her episodes of NSVT.

Even though the QRS complexes seen in leads V1,V2 of Figure-2 are
ventricular — the shape of the ST
depression seen in these leads suggests acute posterior involvement consistent with these cath findings.

Assessment of the Post-ConversionTracing:What Can Be Learned?

As mentioned earlier — this patient was
promptly cardioverted — which resulted in conversion to sinus rhythm, as shown
in the post-conversionECG (inFigure-3).

What
can be learned from
the post-conversion tracing?

Figure-3:Post-conversion tracing.

Discussion
of Figure 3:The Post-Conversion Tracing

The post-conversion tracing shows
restoration of sinus rhythm (upright
conducting P waves in lead II at the tachycardic rate of 115-120/minute).
We note a number of subtle findings:

There is RAD (Right Axis Deviation) —
with an rS predominantly negative QRS complex in lead I. This may reflect LPHB
(Left Posterior HemiBlock)
— especially if it is a new finding in this 70-year old woman who is found to
have acute LCx occlusion.

There is IRBBB ( = incomplete RBBB) — given the predominant R wave in lead V1 plus narrow terminal s waves in leads
I,V6 — but no QRS widening.

The ST elevation that we saw in leads
II,III in Figure-2 seems to have resolved. Small inferior q waves
persist.

There appears to be slight-but-real ST elevation in lead V6
(especially when compared to if anything,
slight ST depression in lead V5). Thus synthesis of ECG findings from
capture beats in Figure-2 plus analysis of the post-conversion tracing in
Figure-3 are consistent with acute infero-postero-lateral STEMI (confirmed by
cath findings of acute dominant LCx occlusion) — that resulted in runs of NSVT.

Figure-4:Comparison of post-conversion QRS morphology (within red rectangles) to the 12-lead ECG during the wide tachycardia.

Discussion
of Figure 4:Comparison of VT with the Post-Conversion
ECG

Given successful treatment of this
patient — We enjoy the luxury of being able to dissect her initialECG ( = Figure-1) by direct comparison with the post-conversion
tracing (Figure-3). We do this in Figure-4 — in which QRS morphology after conversion to sinus
rhythm is shown within RED rectangles
in each of the 12 leads.

Making this lead-by-lead comparison suggests a fascinating finding — namely
that all narrow complexes on this tracing probably represent some slight degree
of fusion rather than being pure “capture”
beats. Therefore — rather than representing a series of short runs of NSVT — we
strongly suspect continuousVTthroughout the entire long lead II
rhythm strip seen in Figure-1!

Note the middle complex within the
GREEN rectangle in lead I of Figure-4. This middle complex is narrow and
all negative. It’s shape is precisely what one would expect to see if the
post-conversion sinus rS complex in lead I (within
the RED rectangle) occurred at the same
time as the all negative QS VT beat did. It makes much more sense that the all
negative narrow QRS within the GREEN rectangle in lead I is a fusion beat —
because it is so rare for sinus beats to manifest an all negative QRS in lead
I. In contrast — the predominantly negative rS complex in lead I of the post-conversion
tracing is perfectly consistent with a LPHB pattern, which is not at all
unexpected given acute occlusion of a dominant LCx artery.

Similarly — there are other subtle
differences in morphology during and after VT in other leads that suggest all narrow
beats in Figure-1 probably represent fusion complexes (ie, loss of the small initial r wave in lead aVL during VT for beat #10 —
and loss of the initial small q wave in lead V6 during VT for beat #23).

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CLICK HERE— for download of a pdf review on assessment of the regular wide tachycardia (excerpted from my ACLS-2013-ePub). Detailed discussion of QRS morphology, axis during tachycardia, and other discriminating criteria is included.